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Yet, studies of gene expression at the tissue level capable of identifying the causes of endocrine dysfunctions are lacking. Transcript levels of endocrine-specific genes were analyzed in five endocrine organs of lethal COVID-19 cases.\u00a0Overall, 116 autoptic specimens from 77 individuals (50 COVID-19 cases and 27 uninfected controls) were included. Samples were tested for the SARS-CoV-2 genome. The adrenals, pancreas, ovary, thyroid, and white adipose tissue (WAT) were investigated. Transcript levels of 42 endocrine-specific and 3 interferon-stimulated genes (ISGs) were measured and compared between COVID-19 cases (virus-positive and virus-negative in each tissue) and uninfected controls.\u00a0ISG transcript levels were enhanced in SARS-CoV-2-positive tissues. Endocrine-specific genes (e.g.,\n                      <jats:italic>HSD3B2<\/jats:italic>\n                      ,\n                      <jats:italic>INS<\/jats:italic>\n                      ,\n                      <jats:italic>IAPP<\/jats:italic>\n                      ,\n                      <jats:italic>TSHR<\/jats:italic>\n                      ,\n                      <jats:italic>FOXE1<\/jats:italic>\n                      ,\n                      <jats:italic>LEP<\/jats:italic>\n                      , and\n                      <jats:italic>CRYGD<\/jats:italic>\n                      ) were deregulated in COVID-19 cases in an organ-specific manner. Transcription of organ-specific genes was suppressed in virus-positive specimens of the ovary, pancreas, and thyroid but enhanced in the adrenals. In WAT of COVID-19 cases, transcription of ISGs and leptin was enhanced independently of virus detection in tissue.\u00a0Though vaccination and prior infection have a protective role against acute and long-term effects of COVID-19, clinicians must be aware that endocrine manifestations can derive from virus-induced and\/or stress-induced transcriptional changes of individual endocrine genes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key messages<\/jats:title>\n                    <jats:p>\u2022 SARS-CoV-2 can infect adipose tissue, adrenals, ovary, pancreas and thyroid.<\/jats:p>\n                    <jats:p>\u2022 Infection of endocrine organs induces interferon response.<\/jats:p>\n                    <jats:p>\u2022 Interferon response is observed in adipose tissue independently of virus presence.<\/jats:p>\n                    <jats:p>\u2022 Endocrine-specific genes are deregulated in an organ-specific manner in COVID-19.<\/jats:p>\n                    <jats:p>\n                      \u2022 Transcription of crucial genes such as\n                      <jats:italic>INS<\/jats:italic>\n                      ,\n                      <jats:italic>TSHR<\/jats:italic>\n                      and\n                      <jats:italic>LEP<\/jats:italic>\n                      is altered in COVID-19.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00109-023-02334-3","type":"journal-article","created":{"date-parts":[[2023,5,29]],"date-time":"2023-05-29T03:02:37Z","timestamp":1685329357000},"page":"973-986","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Transcriptional changes in multiple endocrine organs from lethal cases of COVID-19"],"prefix":"10.1007","volume":"101","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0212-8249","authenticated-orcid":false,"given":"Anello Marcello","family":"Poma","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diana","family":"Bonuccelli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elisabetta","family":"Macerola","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sara","family":"Niballi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alessio","family":"Basolo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ferruccio","family":"Santini","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fulvio","family":"Basolo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonio","family":"Toniolo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2023,5,29]]},"reference":[{"key":"2334_CR1","doi-asserted-by":"publisher","first-page":"312","DOI":"10.1016\/j.it.2021.02.003","volume":"42","author":"C King","year":"2021","unstructured":"King C, Sprent J (2021) Dual nature of type I interferons in SARS-CoV-2-induced inflammation. 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